Highlights
• The CK-CIT and CK-MIT activity were lower in the heart of infected by L. monocytogenes, contributing to the decrease in available ATP for the Na+/K + -ATPase.
• Reduction in activity of phosphotransferases and Na+/K + -ATPase were observed in heart and liver associated with increased lipoperoxidation.
• Lipid peroxidation demonstrates a pronounced oxidizing response and helps to clarify the indirect damage of Na+/K + -ATPase action.
• ACAP levels were higher in the infected group, but it was not able to neutralize lipoperoxidation and regulate phosphotransferase activity.
Abstract
Energy metabolism is a sensitive indicator of cellular disorders. Therefore, the objective of this study was to investigate changes in cardiac and hepatic energy metabolism during listeriosis using an experimental model. We divided gerbils into two groups: Control (n = 11) and orally Infected (n = 12) with 5 × 109 CFU/mL of Listeria monocytogenes. Euthanasia and sampling were performed on days 6 and 12 post-infection (PI). Histopathological lesions were not found in the heart; however, the liver showed pyogranuloma. In the hearts of infected animals, cytosolic creatine kinase activity was lower on day 6 and 12 PI; mitochondrial creatine kinase/pyruvate kinase (PK), and sodium potassium pump (Na+/K+-ATPase) activities were lower on day 12 PI. Hepatic PK and Na+/K+-ATPase activities were lower in the infected group on day 12 PI. Lipoperoxidation was higher in the livers and hearts of infected animals on day 12 PI, and antioxidant capacity against peroxyl radicals (ACAP) was also higher in this group. These data suggest that subclinical listeriosis alters hepatic and cardiac energy metabolism, possibly related to decreased activity of phosphotransferases and ATPase. Subsequent antioxidant responses are not sufficient to correct alterations in lipid peroxidation and bioenergetics, possibly leading to important cellular pathological mechanisms.
